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Войти в исследования Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2025
Aqueous Pistacia lentiscus leaves extract protects against ethanol-induced gastroduodenal ulcers in rat.
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Zahouani Yasmina, Khazri Abdelhafidh, Touaylia Samir, Ben Rhouma Khemais, Sebai Hichem, Sakly Mohsen
Аннотация
BACKGROUND AND AIM: The protective effects of aqueous extract of Pistacia lentiscus leaves (AELPL) against gastric and duodenal ulcers induced by alcohol oral gavage administration in Wistar rats were investigated in this study.
METHODS: The rats were divided into six groups control, ethanol single, ethanol + AEPL (25-50-100) and famotidine + ethanol.
RESULTS: HPLC-MS analysis allowed the identification of numerous phenolic compounds in P. lentiscus leaves such as flavonoids (isoquercetin and luteolin), flavonols (catechin, rutin and kaempferol), phenolic acids (ellagic and dicaffeoylquinic) and tannins. Ethanol administration induced significant gastric and duodenal ulcerative lesions, while AELPL pretreatment (25, 50 and 100 mg/kg) provided a dose-dependent mucosal protection comparable to famotidine, a widely used drug for the treatment of gastric ulcers. AELPL like famotidine also restored gastric pH and volume, counteracting ethanol-induced acidity. Biochemical analyses demonstrated that AELPL like famotidine mitigated oxidative stress by reducing lipid peroxidation, carbonylated proteins and hydrogen peroxide levels, whereas it restored non-protein thiols content in the stomach, duodenum and plasma in a dose-dependent manner. Additionally, AELPL restored antioxidant enzyme activities including catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase. AELPL also reduced ethanol-induced increase in free iron, ionized calcium and interleukin-6 levels, indicating its anti-inflammatory potential.
CONCLUSION: These findings suggest that AELPL exhibits gastroduodenal protective effects against ethanol-induced damage, with efficacy comparable to famotidine. Protective mechanisms likely involve modulation of oxidative stress and inflammation, supporting AELPL's potential as a therapeutic agent for gastroduodenal injuries.
METHODS: The rats were divided into six groups control, ethanol single, ethanol + AEPL (25-50-100) and famotidine + ethanol.
RESULTS: HPLC-MS analysis allowed the identification of numerous phenolic compounds in P. lentiscus leaves such as flavonoids (isoquercetin and luteolin), flavonols (catechin, rutin and kaempferol), phenolic acids (ellagic and dicaffeoylquinic) and tannins. Ethanol administration induced significant gastric and duodenal ulcerative lesions, while AELPL pretreatment (25, 50 and 100 mg/kg) provided a dose-dependent mucosal protection comparable to famotidine, a widely used drug for the treatment of gastric ulcers. AELPL like famotidine also restored gastric pH and volume, counteracting ethanol-induced acidity. Biochemical analyses demonstrated that AELPL like famotidine mitigated oxidative stress by reducing lipid peroxidation, carbonylated proteins and hydrogen peroxide levels, whereas it restored non-protein thiols content in the stomach, duodenum and plasma in a dose-dependent manner. Additionally, AELPL restored antioxidant enzyme activities including catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase. AELPL also reduced ethanol-induced increase in free iron, ionized calcium and interleukin-6 levels, indicating its anti-inflammatory potential.
CONCLUSION: These findings suggest that AELPL exhibits gastroduodenal protective effects against ethanol-induced damage, with efficacy comparable to famotidine. Protective mechanisms likely involve modulation of oxidative stress and inflammation, supporting AELPL's potential as a therapeutic agent for gastroduodenal injuries.